Inflammatory Proteins in Plasma Are Associated with Severity of Alzheimer’s Disease
Open accessAbstract
Markers of Alzheimer's disease (AD) are being widely sought with a number of studies suggesting blood measures of inflammatory proteins as putative biomarkers. Here we report findings from a panel of 27 cytokines and related proteins in over 350 subjects with AD, subjects with Mild Cognitive Impairment (MCI) and elderly normal controls where we also have measures of longitudinal change in cognition and baseline neuroimaging measures of atrophy. In this study, we identify five inflammatory proteins associated with evidence of atrophy on MR imaging data particularly in whole brain, ventricular and entorhinal cortex measures. In addition, we observed six analytes that showed significant change (over a period of one year) in people with fast cognitive decline compared to those with intermediate and slow decline. One of these (IL-10) was also associated with brain atrophy in AD. In conclusion, IL-10 was associated with both clinical and imaging evidence of severity of disease and might therefore have potential to act as biomarker of disease progression.
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Pathways involving mitochondrial dysfunction or inflammation have been linked to rapid progression, but these associations may be downstream effects of true drivers of progression.
“While pathways involving mitochondrial dysfunction or inflammation have been linked to rapid progression, these proteomic and physiological associations may be downstream effects of true drivers of progression [9–11].”
From Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk (2026) · cites this paper as [10]
The Results section links changes in inflammatory proteins to fast cognitive decline in Alzheimer’s disease. The Discussion asks whether the peripheral inflammatory signature is secondary to inflammation in the brain, but does not establish that these associations are downstream effects of the drivers of progression. This paper does not address mitochondrial dysfunction. (LLM, conf=0.82)
Experimental — accuracy not yet measuredElevated CCL11 may contribute to driving neovascularisation in AMD via interaction with CCR3.
“Elevated CCL11 in the plasma and cerebrospinal fluid seen in aging mice and humans are associated with declining neurogenesis, neurodegenerative disease, and cognitive decline and may contribute to driving neovascularisation in AMD via interaction with CCR3 [1, 93, 123].”
From Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain (2022) · cites this paper as [93]
Elevated CCL11 in the plasma and cerebrospinal fluid seen in aging mice and humans are associated with declining neurogenesis, neurodegenerative disease, and cognitive decline.
“Elevated CCL11 in the plasma and cerebrospinal fluid seen in aging mice and humans are associated with declining neurogenesis, neurodegenerative disease, and cognitive decline and may contribute to driving neovascularisation in AMD via interaction with CCR3 [1, 93, 123].”
From Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain (2022) · cites this paper as [93]
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- Authors
- Leung, R., Proitsi, P., Simmons, A., Lunnon, K., Güntert, A., Kronenberg, D., Pritchard, M., Tsolaki, M., Mecocci, P., Kloszewska, I., Vellas, B., Soininen, H., Wahlund, L.-O., & Lovestone, S.
- Affiliations
- King's College London (GB)
- Aristotle University of Thessaloniki (GR)
- University of Perugia (IT)
- Inserm (FR)
- University of Eastern Finland (FI)
- Corresponding author
- Lovestone, Simon
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-06-10
- Volume
- 8
- Issue
- 6
- Pages
- e64971
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3677891
- OpenAlex
- W2086474013
- Cited by
- 160
- References
- 43
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 18 · 2023: 12 · 2022: 13 · 2021: 19 · 2020: 13 · 2019: 9 · 2018: 15 · 2017: 10 · 2016: 6 · 2015: 15 · 2014: 9 · 2013: 2
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Open Research Exeter (University of Exeter) (publishedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- South London and Maudsley NHS Foundation Trust
- Wellcome Trust (100140)
- National Institute for Health and Care Research (NF-SI-0512-10053)
- King's College London
- European Commission (FP6-2004-LIFESCIHEALTH-5)
- Medical Research Council
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, inflammatory proteins, cytokines, biomarkers, disease severity, mild cognitive impairment, brain atrophy, entorhinal cortex, ventriculomegaly, IL-10, cognitive decline, disease progression, neuroimaging
- MeSH terms
- Aged, Alzheimer Disease, Atrophy, Brain, Cognition Disorders, Enzyme-Linked Immunosorbent Assay, Female, Humans, Magnetic Resonance Imaging, Male, Prognosis, Severity of Illness Index, Cohort Studies, Biomarkers, Case-Control Studies, Cytokines, Disease Progression, Inflammation Mediators, Functional Neuroimaging
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